PurposeCarfilzomib has been approved for use in relapsed and refractory multiple myeloma (RRMM). Cardiac toxicities have been reported with the use of carfilzomib. We aimed to determine the overall incidence and risk of cardiac toxicities in RRMM patients treated with carfilzomib using a meta-analysis.MethodsWe searched several databases for relevant articles. Prospective trials evaluating carfilzomib in RRMM patients with adequate data on cardiac toxicities were included for analysis. Pooled incidence, Peto ORs, and 95% CIs were calculated according to the heterogeneity of selected studies.ResultsA total of 2,607 RRMM patients from eight prospective trials were included. The pooled incidence of all-grade congestive heart failure (CHF) and ischemic heart disease (IHD) related to carfilzomib in RRMM patients was 5.5% (95% CI: 4.3%–6.9%) and 2.7% (95% CI: 1.1%–6.7%), respectively. In addition, the use of carfilzomib significantly increased all-grade (Peto OR 2.33, 95% CI: 1.56–3.48, p<0.001) and high-grade (Peto OR 3.22, 95% CI: 1.84–5.61, p<0.001) CHF when compared to controls, whereas there was no significantly increased risk of developing all-grade (Peto OR 1.31, 95% CI: 0.79–2.18, p=0.30) and high-grade (Peto OR 1.41, 95% CI: 0.73–2.72, p=0.31) IHD in RRMM patients receiving carfilzomib.ConclusionThe use of carfilzomib in RRMM patients significantly increases the risk of developing CHF but not IHD. Clinicians should be cautious about the risk of CHF associated with carfilzomib to maximize the benefits and minimize the toxicities.

Objective. To investigate the clinical significance and safety of interferon in the treatment of chronic myeloproliferative tumors (MPN). Methods. In this prospective study, a total of 120 patients with advanced chronic MPN admitted to our hospital between April 2016 and August 2020 were assessed for eligibility and recruited, including 62 patients with JAK2V617F mutation-positive ET (ET group) and 58 patients with JAK2V617F mutation-positive PV (PV group). 62 patients with JAK2V617F mutation-positive ET were assigned (1 : 1) to receive interferon-α (IFN-α) or hydroxyurea (HU). A similar subgrouping method for treatment of IFN-α and HU was introduced to patients with JAK2V617F mutation-positive PV. Outcome measures included efficacy and adverse reactions. Results. For patients with JAK2V617F mutation-positive ET and PV, there were no significant differences in the overall response rate between the groups treated with IFN-α or HU ( P > 0.05 ); however, the patients treated with IFN-α had a significantly higher 5-year progression-free survival (PFS) than those treated with HU ( P < 0.05 ). IFN-α was associated with a significantly lower incidence of disease progression, thrombotic events, splenomegaly, myelofibrosis, nausea, and vomiting and a higher incidence of hematological adverse reactions and flu-like symptoms versus HU ( P < 0.05 ). After six months of treatment, the PV group had 12 cases of hematological response both in the IFN-α subgroup and the HU subgroup and fewer PV patients treated with IFN-α required phlebotomy versus those treated with HU ( P < 0.05 ), in which 4 patients in the IFN-α subgroup had no hematological response and 6 patients in the HU subgroup had no hematological response. There was no significant difference in the number of cases with phlebotomy between the two subgroups of PV patients without hematological response ( P > 0.05 ). Conclusion. The use of IFN in the treatment of JAK2V617F mutation-positive ET and PV patients yields a prominent clinical effect by prolonging PFS and avoiding phlebotomy for JAK2V617F mutation-positive PV patients.